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Sesamin suppresses NSCLC cell proliferation and induces apoptosis via Akt/p53 pathway

Yueming Chen1, Huachao Li1, Weinan Zhang1

  • 1Department of Clinical Pharmacy, School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, China; Guangzhou key laboratory of construction and application of new drug screening model systems, Guangdong Pharmaceutical University, Guangzhou 510006, China; Key Laboratory of New Drug Discovery and Evaluation of ordinary universities of Guangdong province, Guangdong Pharmaceutical University, Guangzhou 510006, China.

Toxicology and Applied Pharmacology
|December 7, 2019
PubMed

Insights

Sesamin effectively combats non-small cell lung cancer (NSCLC) by halting cell growth and promoting cell death. This natural compound targets the Akt/p53 pathway, offering potential as an NSCLC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Non-small cell lung cancer (NSCLC) presents a significant clinical challenge due to its high prevalence and poor patient outcomes.
  • Investigating novel therapeutic agents for NSCLC is crucial for improving treatment efficacy.

Purpose of the Study:

  • To elucidate the anticancer properties of sesamin against NSCLC cells.
  • To investigate the molecular mechanisms underlying sesamin's anti-NSCLC effects, focusing on cell cycle regulation, apoptosis, and key signaling pathways.

Main Methods:

  • Cell proliferation was assessed using MTT assays.
  • Cell cycle distribution and apoptosis were analyzed via flow cytometry.
  • Protein expression and activation of key molecules (Akt, p53, cyclin D1, CDK2) were determined by Western blotting and immunohistochemistry (IHC).

Main Results:

  • Sesamin demonstrated dose-dependent suppression of NSCLC cell proliferation and induced apoptosis.
  • Sesamin treatment resulted in G1 phase cell cycle arrest, decreased cyclin D1 and CDK2 expression, and inhibited Akt activity while upregulating p53.
  • In vivo studies corroborated in vitro findings, with minimal observed toxicity in major organs.

Conclusions:

  • Sesamin effectively inhibits NSCLC progression by inducing G1 cell cycle arrest and apoptosis.
  • The Akt/p53 signaling pathway is a critical mediator of sesamin's anti-NSCLC effects.
  • Sesamin holds promise as a potential adjuvant therapeutic agent for non-small cell lung cancer.
Keywords:
ApoptosisCell cycle arrestCyclin D1NSCLCSesaminp53

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